The effects of 2,3-diphosphoglycerate, adenosine triphosphate, and glycosylated hemoglobin on the hemoglobin-oxygen affinity of diabetic patients

The position of the oxygen dissociation curve (ODC) is modulated by 2,3-diphosphoglycerate (2,3-DPG). Decreases in 2,3-DPG concentration within the red cell shift the curve to the left, whereas increases in concentration cause a shift to the right of the ODC. Some earlier studies on diabetic patients have reported that insulin treatment may reduce the red cell concentrations of 2,3-DPG, causing a shift of the ODC to the left, but the reports are contradictory. Three groups were compared in the present study: 1) nondiabetic control individuals (N = 19); 2) insulin-dependent diabetes mellitus (IDDM) patients (on insulin treatment) (N = 19); 3) non-insulin-dependent diabetes mellitus (NIDDM) patients using oral hypoglycemic agents and no insulin treatment (N = 22). The overall position of the ODC was the same for the three groups despite an increase of the glycosylated hemoglobin fraction that was expected to shift the ODC to the left in both groups of diabetic patients (HbA1c: control, 4.6 percent; IDDM, 10.5 percent; NIDDM, 9.0 percent). In IDDM patients, the effect of the glycosylated hemoglobin fraction on the position of the ODC appeared to be counterbalanced by small though statistically significant increases in 2,3-DPG concentration from 2.05 (control) to 2.45 æmol/ml blood (IDDM). Though not statistically significant, an increase of 2,3-DPG also occurred in NIDDM patients, while red cell ATP levels were the same for all groups. The positions of the ODC were the same for control subjects, IDDM and NIDDM patients. Thus, the PO2 at 50 percent hemoglobin-oxygen saturation was 26.8, 28.2 and 28.5 mmHg for control, IDDM and NIDDM, respectively. In conclusion, our data question the idea of adverse side effects of insulin treatment on oxygen transport. In other words, the shift to the left reported by others to be caused by insulin treatment was not detected

Regulation of acid-base status in ectothermic vertebrates: the consequences for oxygen pressures in lung gas and arterial blood

Extensive literature reports a negative deltapHa/deltat in ectothermic vertebrates, but data are scarce as to its consequences for O2 transport. In reptiles, the negative delta-pHa/delta-t results from an elevated lung gas PCO2 (PACO2) at higher temperatures, implying a corresponding fall of PAO2. In parallel, arterial PO2 rises with temperature, due to a combination of central vascular shunt and decreasing Hb O2 affinity. As a result, the PO2 gradient between lung gas and blood (PA-aO2) becomes reduced at higher temperatures. In amphibians, the negative delta-pHa/delta-t results from combined cutaneous and pulmonary CO2 elimination. We propose that this leads to a rather temperature-independent lung gas PO2. Moreover, our calculations suggest that resting reptiles and amphibians maintain a relatively large PA-aO2 also at high temperatures. The negative delta-pHa/delta-t in teleost fish is generally considered to be a result of modulated plasma [HCO3-]. Recent data from our laboratory suggest that acute pH adjustments at high temperatures may involve alterations of PaCO2 through gill ventilation, leading to a decrease of PaO2 with rising temperature.